Jump to content

User:Dirkster07/sandboxAddiction

From Wikipedia, the free encyclopedia

Introduction to Addiction

[edit]

Addiction is defined as the continued use of a mood altering substance or behaviour despite adverse consequences. [1] This can include, but is not limited to alcohol abuse, drug abuse, exercise abuse, and gambling. Some defining characteristics the addiction include impaired control over subtances/behaviour, preoccupation with substance/behaviour, continued use despite consequences, and denial.[2] Habits and patterns associated with addiction are typically characterized by immediate gratification (short-term reward), coupled with delayed deleterious effects (long-term costs). [3]Physiological dependence occurs when the body has to adjust to the substance by incorporating the substance into its 'normal' functioning [4]. This state creates the conditions of tolerance, and withdrawal. Tolerance is the process by which the body continually adapts to the substance and requires increasingly larger amounts to achieve the original effects. Withdrawal refers to physical and psychological symptoms people experience when reducing or discontinuing a substance the body had become dependent on. Symptoms of withdrawal generally include but are not limited to anxiety, irritability, intense cravings for the substance, nausea, hallucinations, headaches and tremors.

Biological Mechanisms

[edit]

This section will briefly discuss the biological mechanisms involved in addiction, such as the dopamine response model and genetic markers.

Cognitive Theories of Addiction

[edit]

This section will very briefly discuss the role of cognition in addiction

Personality Theories of Addiction

[edit]

Role of Affect Dysregulation in Addiction

[edit]

Research has consistently shown strong associations between affect and substance use disorders. Specifically, people with affect mood disorders are at increased risk of substance use disorders.[5] Affect and addiction can be related in a variety of ways as they play a crucial role in influencing motivated behaviours. For instance, affect facilitates action, directs attention, prepares the individual for a physical response, and guides behaviour to meet particular needs.[6] Moreover, affect is implicated in a range of concepts relevant to addiction: negative and positive reinforcement, behaviour motivation, regulation of cognition and mood, and reasoning and decision making.[7][8] Emotion-motivated reasoning has been shown to influence addictive behaviours via selecting outcomes that minimize negative affective states while maximizing positive affective states.[9]

Negative Affect
[edit]

The relationship between negative affect and substance use disorders has been the most widely studied model of addiction. It proposes that individuals who experience the greatest levels of negative affect are at the greatest risk of using substances/behaviours as a coping mechanism.[10][11] Here, substances and behaviours are used to improve mood and distract from unpleasant feelings. Once physical dependence has been established, substance abuse is primarily motivated by a desire to avoid negative affective states associated with withdrawal. Individuals high in affective mood disorders (anxiety) most commonly report high levels of negative affect associated with cravings.[12][13][14] However, the relationship between negative affect and addiction is not unidirection. Meaning, while negative affect increase the likelihood of initiation of substance use, the negative affective states produced by withdrawal are the most commonly reported factors for continued use.[5] Key to this concept is the 'Hedonic Hypothesis' which states that individuals initiate use of the substance/behaviour for their pleasurable effects, but then take it compulsively to avoid withdrawal symptoms, resulting in dependence.[15] Based on this hypothesis it is believed that individuals engaging in risky use of substances/behaviours may be over-responsive to negative stimuli which leads to addiction.

Negative affect has also been a powerful predictor in terms of vulnerability to addiction in adolescents. High risk adolescents have been found to be highly reactive to negative stimuli, which increases their motivation to engage in substance use following a negative emotion-arousing situation.[16] Moreover, it has been established that adolescents high in negative affect are at increased risk for moving from recreational use to problematic use despite a family history of addiction.[16] Furthermore, the trait 'negative urgency', the propensity to engage in risky behaviour in response to distress, is highly predictive of certain aspects of substance abuse in adolescents.[17] Early individual differences in emotional differences in reactivity and regualtion underlie the later emergence of the trait 'negative urgency'.[18]

Positive Affect
[edit]

Unlike negative affect, positive affect is related to addiction in both high and low forms. For example, individuals high in positive affect are more likely to engage in risky behaviour, such as drug use. Also, individuals with high positive affect in response to use are more likely to seek out substances for hedonic reasons. Conversely, low positive affect may prompt initial use due to lack or responsiveness to natural rewards.[5]

Extensive personality research has been done that links positive emotional states to individual differences in risky behaviour.[5] The trait 'positive urgency' , the tendency to engage in risky behaviour under conditions of extreme positive affect, is predictive of substance/behavioural problems that lead to addiction.[19] This trait represents an underlying dysregulation in response to extreme affective states and has a direct impact on behaviour. The trait 'positive urgency' has been shown to have a predictive relationship with increases in drinking quantity and alcohol related problems in college, drug use in college.[17][20] Furthermore this trait provides important information on how positive affect can increase the likelihood of engaging in substance abuse. Another important factor to consider is individual differences in the experience of pleasurable effects brought on by the substance/behaviour. It is reasoned that certain individuals may be more sensitive to the pleasurable effects, and thus experience them with greater intensity resulting in addiction.[5] For example, over-responsiveness to substance affects has been found in cocaine addicts - an increased response to methylphenidate in the brain regions associated with emotional reactivity and mood.[21][22][23] Thus, strong emotional responses that addicted individuals show in response to substances/behaviours might be a results of enhanced sensitivity to their effects.

Individuals differ in the way by which they metabolize substances, such as alcohol, these positive reinforcing effects are predetermined.[5] Individual reactivity to the effects of substances may effect motivation to use. For example, if a person experiences strong positive (and weak negative) effects from a substance, due to their biochemical profile, their expectations of the positive effects from the substance will be heightened. Therefore, increasing their desire to for continued use, resulting in dependence.[5] According to this model, the experience of the positive mood enhances implicit attention to substance cues and implicit associations between reward and substance use.[24]

Interestingly, many addicts report symptoms of anhedonia; the inability to experience pleasure.[25] Results of chronic deviation of the brain's reward set point, following prolonged intoxication, diminish responsivity to natural positive stimuli.This may result in an over-responsiveness to substance related cues, coupled with an impaired capacity to initiate behaviours in response to natural rewards.[26] Low positive affect, thus, inhibits the individuals ability to replace drug taking with other rewarding activities. It has also been proposed that during substance dependence the somatic states that guide decision making are weakened in relation to natural rewards, while at the same time enhances the emotional response to drug-related stimuli.[27]

Compulsive behaviours characterized by addiction are underpinned by two interacting systems: (a) impulsivity, and (b) Reflection. Impulsivity is responsible for the rapid signalling of the affective importance of a stimuli. While reflection cognitively evaluates the signal before altering the behavioural response. Dysfunction in impulsivity exaggerates the emotional impact of the drug-related stimuli and attenuates the impact of natural reinforcement.[5] Dysregualtion in reflection results in the inability to override impulsivity; thus resulting in addiction.[5] Under-responsiveness to naturally occurring positive stimuli is a crucial element that biases the individual towards the use of substances/behaviours and away from non-drug alternatives.

Effortful Control
[edit]

Tempermental effortful control is defined as the ability to suppress a dominant response in order to perform a subdominant response.[28] In other words, it is the degree of control the individual has over impulses and emotions; which includes the ability to focus or shift attention. Tempermental effortful control can influence addiction in a number of ways. Low levels of effortful can render the individual less able to distract themselves from unpleasant feelings or overcome strong affective impulses, resulting in maladaptive responses to distress - such as continued substance use.[5] Low effortful control may also interact with negative and positive affect, predisposing the individual to substance/behavioural use, and impair their ability to control use.[5] A general inability to control affective states may impair the conditioning of behaviour associated with rewards and punishment, increase susceptibility to biasing by substance-related cues, and could tax self-regulatory capacity.[5] Thus, leaving the individuals unable to interrupt automatic drug-seeking behaviours. Abnormal levels of positive and negative affect can be increased by low effortful control.[29][30] For example, high positive affect may interact with low effortful control in increasing risk of addiction amongst vulnerable populations.


Gray's Reinforcement Sensitivity Theory

[edit]

Gray's Reinforcement Sensitivity Theory (RST) consists of two motivational systems, the Behaviour Inhibition System (BIS) and the Behaviour Activation System (BAS).[31][32] The BIS is responsible for organizing behaviour in response to adverse stimuli. In other words, stimuli associated with punishment or the omission/termination of reward, and pustulated to underlie anxiety. The purpose of the BIS is to initiate behaviour inhibition, or interrupt ongoing behaviour, while the BAS was sensitive to stimuli that signal reward and/or relief from punishment (impusivity).[31] [32] In accordance with the RST, an association was found between people with extreme scores in BIS/BAS and adjustment problems. BIS and BAS reactivity correspond with individual trait differences in positive affect and negative affect - The BAS is associated with trait impulsivity and positive affect, while the BIS is associated with trait negative affect.[33] [34] For instance, it has been postulated that high BIS is related to anxiety, while high BAS is related to conduct disorders or impulsivity. [32] [35] According to this model substance abuse problems may arise under two different personality traits: low BIS and high BAS. Since the BAS promotes the individual to pursue actions that may result in reward, BAS sensitivity is involved in the initiation of addiction. Significant associations have been found between high BAS alcohol misuse in school girls, hazardous drinking in men, illicit drug abuse, and tobacco use. BAS sensitivity is a significant predictor of reactivity to substance cues, or cravings.[36][37][38][39][40][41][42][43][44][45] Conversely, BIS sensitivity is involved in avoiding negative situations or affect (such as withdrawal). Low BIS has been positively associated with continuing the addiction to relieve feelings of withdrawal, or for continued use to alleviate negative affect.


Model of Impulsivity

[edit]

The model of impulsivity states that individuals high in impulsivity are at greater risk of addictive behaviours. The model proposes a two dimensional trait characteristic for the initiation and continuation of substance/behavioural abuse. The first trait discussed is Reward Drive (RD), and reflects individual differences in sensitivities to incentive motivation and engagement of addictive behaviour when reward cues are detected. [46] The second trait described by the model is Rash Impulsiveness (RI), reflecting individual differences in the ability to modify the addictive behaviour due to negative consequences. [46] Individuals high in RI are oblivious or insensitive to the negative consequences as a result of addictive behaviour when engagement is craved. Both high RD and RI individuals are found to have difficulty in making decisions that have future consequences. Individuals high in RD experience greater reinforcement when initially engaging in the addictive behaviour, and experience stronger conditioned associations with continued use. Individuals high in RI experience greater difficulty resisting cravings even in the face of negative consequences. [46] Some moderators of RD and RI on the severity of addiction are stress and negative affect (such as feeling depressed). [47] That is, individuals high in RD/RI who also experience high levels of negative affect or stress, present more severe addictive behaviours. For example, if an individual is experiencing emotional distress, the distress experienced may lessen impulse control if they believe that engaging in addictive behaviour will decrease negative affect. According to this model, adolescents who are high in RI are at greater risk for developing addictions. Interestingly, low RI has been shown to moderate some of the risk of addiction due to family history. [48][49][50][51] However, high RI for individual without a family history of addiction has been related to poor decision making.


Cloninger's Tri-Dimensional Personality Theory

[edit]

Cloninger's Tri-Dimensional Personality Theory states that personality is comprised of three genetically independent dimensions: (a) Novelty seeking (NS): tendency towards exploration and intense exhilaration in response to novel stimuli, (b) Harm avoidance (HA):intense response to adverse stimuli and learned inhibited behaviour to avoid punishment , and (c) Reward dependence (RD): resistance to extinction of previously rewarded behaviour.[52] Each personality dimension lies on a spectrum ranging from low to high. For example, individuals high in NS are impulsive, while individual's low in NS are reflective. Interactions between each of these three personality dimensions lead to different responses to novelty, punishment and rewards.[52]

This model was extended to alcohol use disorders proposing that individuals with alcohol use disorders have extreme temperaments (i.e. are very high or very low in NS, HA, and RD). [53] This model proposes that alcoholics can be classified in two groups based on the combinations of their three personality dimensions.[52] Type I alcoholics have a late onset of alcohol related problems, experience guilt and fear associated with consumption, lose control once drinking is initiated, engage in alcohol related antisocial conduct, and rarely exhibit spontaneous alcohol-seeking behaviour.[54] Type I alcoholics are thought to be low in NS and high in HA and RD - emotionally dependent, rigid, perfectionistic, anxious, quiet, patient, and introverted.[54] Unlike Type I alcoholics, Type II alcoholics have an earlier onset of alcohol related problems, less ability to abstain from alcohol, more frequent alcohol-related antisocial behaviour, less loss of control once drinking commenced, and less guilt or fear associated with drinking.[54] These individuals are high in NS, and low in HA and RD. Meaning, they are aggressive, impulsive, active, talkative, and impatient.[54]

References

[edit]
  1. ^ Angres D.H., Bettinardi-Angres K (2008). The Disease of Addiction: Origins, Treatment, and Recovery. Disease-a-Month, 54 (10), 696-721
  2. ^ Morse R, Flavin D (1992). The Definition of Alcoholism. Journal of American Medical Association, 268, 1035-1039
  3. ^ Marlatt G.A., Baer J.S., Donovan D.M., Kivlahan D.R. (1988). Addictive Behaviours: Etiology and Treatment. Ann. Rev. Psychol, 39, 223-252
  4. ^ Torres G, Horowitz I.M. (1999). Drugs of abuse and brain gene expression. Psychosomatic Medicine, 61, 630-650
  5. ^ a b c d e f g h i j k l Cheetham A, Allen N, Yucel M, Lubman D (2010). The Role of Affective Dysregulation in Drug Addiction. Clinical Psychology Review, 30, 621-634
  6. ^ Gross J.J. (1998). The emerging field of emotion regulation: An integrative review. Review of General Psychology. Special Issue: New Directions in Research on Emotion, 2(3), 271-299
  7. ^ Bechara A, Damasio H (2002). Decision-making and addiction (part 1): Impaired activation of somatic states in substance dependent individuals when pondering decisions with negative future consequences. Neuropsychologia, 40(10), 1675-1689
  8. ^ Quirk S.W. (2001). Emotion concept models of substance abuse. Drug and Alcohol Review, 20(1), 95-104
  9. ^ Western D, Blagov P.S., Harenski K, Kilts C, Hamann S (2006). Neural basis of motivated reasoning: An fMRI study of emotional constraints on partisan political judgement in the 2004 U.S. presidential election. Journal of Cognitive Neuroscience, 18(11), 1947-1958
  10. ^ McCollam J.B., Burish T.G., Maitso S.A., Sobell M.B. (1980). Alcohol's effects on psychological arousal and self-reported affect and sensations. Journal of Abnormal Psychology, 89(2), 224-233
  11. ^ Measelle J.R., Stice E, Springer D.W. (2006). A prospective test of negative affect model of substance abuse: Moderating effects of social support. Psychology of Addictive Behaviors, 20(3), 225-233
  12. ^ Childress A.R., Ehrman R, McLellan A.T., MacRae J. (1994). Can induced moods trigger drug-related responses in opiate abuse patients? Journal of Substance Abuse Treatment, 11(1), 17-23
  13. ^ Cooney N.I., Litt M.D., Morse P.A., Bauer L.O., Gaupp L. (1997). Alcohol cue reactivity, negative-mood reactivity, and relapse in treated alcoholic men. Journal of Abnormal Psychology, 106(2), 243-250
  14. ^ Fox H.C., Bergquist K.L., Hong K.I., Sinah R. (2007). Stress-induced and alcohol cue-induced craving in recently abstinent alcohol dependent individuals. Alcoholism, Clinical and Experimental Research, 31(3), 395-403
  15. ^ Robinson T.E., Berridge K.C. (2003). Addiction. Annual Review of Psychology, 54, 25-53
  16. ^ a b Randall D.M., Cox W.M.(2001). Experimental mood inductions in persons at high and low risk for alcohol problems. American Journal of Drug and Alcohol Abuse, 27, 183-187
  17. ^ a b Cyders M.A., Smith G.T., Spillane N.S., Fischer S, Annus A.M., Peterson C. (2007). Integration of impulsivity and positive mood to predict risky behavior: Development and validation of a measure of positive urgency. Psychological Assessments, 19(1), 107-118
  18. ^ Whiteside S.P., Lynam D.R. (2001). The Five Factor Model and impusivity: Using a structural model of personality to understand impulsivity. Personality and Individual Differences, 30(4), 669-689
  19. ^ Cyders M.A., Smith G.T. (2008). Emotion-based dispositions to rash action: Positive and negative urgency. Psychological Bulletin, 134(6), 807-828
  20. ^ Zapolski T.C.B, Cyders M.A., Smith G.T. (2009). Positive urgency predicts illegal drug use and risky sexual behavior. Psychology of Addictive Behaviors, 23(2), 348-354
  21. ^ Volkow N.D, Wang G.J., Fowler J.S., Logan J, Gatley S.J., Gifford A (1999). Prediction of reinforcing responses to psychostimulants in humans by brain dopamine D2 receptor levels. American Journal of Psychiatry, 156(9), 1440-1443
  22. ^ Volkov N.D. (2004). The reality of comorbidity: Depression and drug abuse. Biological Psychiatry, 56(10), 714-717
  23. ^ Volkov N.D., Wang G.J., Ma Y., Fowler J.S., Wong C, Ding Y.S. (2005). Activation of orbital and medial prefrontal cortex by methylphenidate in cocaine addicted subjects but not in controls: Relevance to addiction. Journal of Neuroscience, 25(15), 3932-3939
  24. ^ Cox W.M., Klinger E. (1988). A motivational model of alcohol use. Journal of Abnormal Psychology. Special Issue:Models of Addiction, 97(2), 168-180
  25. ^ Janiri L, Martinotti G, Dario T, Reina D, Paparello F, Pozzi G (2005). Anhedonia and substance-related symptoms in detoxified substance-dependent subjects: A correlation study. Neuropsychobiology, 25, 37-44
  26. ^ Koob G.F., Le Moal M. (1997). Drug abuse: Hedonic homeostatic dysregulation. Science, 278(5335), 52-58
  27. ^ Bechara A. (2003). Risky business: Emotion, decision-making, and addiction. Journal of Gambling Studies, 19(1), 23-51
  28. ^ Rothbart M.K., Ellis I.K, Rueda M.R., Posner M.I. (2003). Developing mechanisms of temperamental effortful control. Journal of Personality, 71(6), 1113-1143
  29. ^ Colder C.R., Chassin L. (1997). Affectivity and impulsivity: Temperament risk for adolescent alcohol involvement. Psychology of Addictive Behaviours, 11(2), 83-97
  30. ^ Hussong A.M, Chassin L. (1994). The stress-negative affect model of adolescent alcohol use: Disaggregating negative affect. Journal of Studies on Alcohol, 55(6), 707-718
  31. ^ a b Gray J.A (1970). The psychophysiological basis of introversion-extraversion. Behaviour Research and Therapy, 8, 249-266
  32. ^ a b c Gray J.A. (1982). The neuropsychology of anxiety: An inquiry into the functions of the septal-hippocampal system. Oxford: Oxford University Press
  33. ^ Campbell-Sills L, Liverant G.I., Brown T.A. (2004). Psychometric evaluation of the behavioral inhibition/behavioral activation scales in a large sample of outpatients with anxiety and mood disorders. Psychological Assessment, 16, 244-254
  34. ^ Jorm A.F., Christensen H, Henderson A.S., Jacomb P.A., Korten A.E., Rodgers B (1999). Using BIS/BAS scales to measure behavioral inhibition and behavioral activation: Factor structure, validity and norms in a large community sample. Personality and Individual Differences, 26, 49-58
  35. ^ Quay H.C. (1997). Inhibition and attention deficit hyperactivity disorder. Journal of Abnormal Child Psychology, 25, 7-13
  36. ^ Franken I, Muris P (2006). BIS/BAS personality characteristics and college students' substance use. Personality and Individual Differences, 40, 1497-1503
  37. ^ Franken I, Muris P, Georgieva I (2006). Gray's model of personality and addiction. Addictive Behaviors, 31, 399-403
  38. ^ Genovese J, Wallace D (2007). Reward sensitivity and substance abuse in middle school and high school students. Journal of Genetic Psychology, 168, 465-469
  39. ^ Hundt N, Kimbrel N, Mitchell J, Nelson-Gray R (2008). High BAS, but not low BIS, predicts externalizing symptoms in adults. Personality and Individual Differences, 44, 563-573
  40. ^ Kimbrel N, Nelson-Gray R, Mitchell J (2007). Reinforcement sensitivity and maternal style as predictors of psychopathology. Personality and Individual Differences, 42, 1139-1149
  41. ^ Knyazev G.G. (2004). Behavioral activation as a predictor of substance use: Mediating and moderating role of attitudes and social relationships. Drug and Alcohol Dependence, 75, 309-321
  42. ^ Loxton N.J., Dawe S (2006). Reward and punishment sensitivity in dysfunctional eating and hazardous drinking women: Associations with family risk. Appetite, 47, 361-371
  43. ^ Loxton N.J., Dawe S (2007). How do dysfunctional dysfunctional eating and hazardous drinking women perform on behavioral measures of reward and punishment sensitivity? Personality and Individual Differences, 42, 1163-1172
  44. ^ O'Connor R.M., Stewart S.H., Watt M.C. (2009). Distinguishing BAS risk for university students's drinking, smoking, and gambling behaviors. Personality and Individual Differences, 46, 514-519
  45. ^ Pardo Y, Aguilar R, Molinuevo B, Torrubia R (2007). Alcohol use as a behavioral sign of disinhibition: Evidence from J.A. Gray's model of personality. Addictive Behaviors, 32, 2398-2403
  46. ^ a b c Dawe S, Loxton N.J. (2004). The role of impulsivity in the development of substance use and eating disorders. Neuroscience and Behavioral Reviews, 28, 343-351
  47. ^ Koob G.F., Le Moal M. (2001). Drug addiction, dysregulation of reward, and allostasis. Neuropsychopharmacology, 24, 97-129
  48. ^ Brook J.S, Kessler R.C., Cohen P. (1999). The onset of marijuana use from pre-adolescence and early adolescence to young adulthood. Development and Psychopathology, 11, 901-914
  49. ^ Lynskey M.T., Fergusson D.M., Horwood L.J. (1998). The origins of the correlations between tobacco, alcohol, and cannabis use during adolescence. Journal of Child Psychology and Psychiatry and Allied Disciplines, 39, 995-1005
  50. ^ King K.M., Chassin L (2004). Mediating and moderating effects of adolescent behavioral undercontrol and parenting in the prediction of drug use disorders in emerging adulthood. Psychology of Addictive Behaviors, 18, 239-249
  51. ^ Tarter R.E., Kirisci L., Habeych M., Reynolds M., Vanyukov M (2004). Neurobehaviour disinhibition in childhood predisposes boys to substance use disorder by young adulthood: direct and mediating etiologic pathways. Drug and Alcohol Dependence, 73, 121-132
  52. ^ a b c Cloninger C.R.A (1987). A systematic method for clinical descriptions and classification of personality variants. Arch. Gen. Psychiat., 44, 573-588.
  53. ^ Howard M.O, Kivlahan D, Walker, B.D. (1997). Cloninger's tridimensional theory of personality and psychopathology: applications to substance use disorders. Journal of Studies on Alcohol, 58.1, 48-71
  54. ^ a b c d Cloninger C.R. (1987b). Neurogenetic adaptive mechanisms in alcoholism. Science, 236, 410-416
Retrieved from "http://en.wiki.x.io/w/index.php?title=User:Dirkster07/sandboxAddiction&oldid=481708252"